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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dynamics of acute mitral regurgitation were studied in six open-chest dogs in whom a portion of the anterior leaflet was excised. Phasic mitral and aortic flows were measured electromagnetically and left ventricular filling volume, regurgitant volume (RV) and forward stroke volume (SV) were calculated. The systolic pressure gradient (SPG) between the left ventricle (LV) and left atrium (LA) was obtained from high-fidelity pressure transducers. The effective mitral regurgitant orifice area (MRA) was calculated from the hydraulic equation of Gorlin. Volume infusion resulted in significant increases in both left atrial and left ventricular pressures; thus, the SPG was unchanged and the increase in RV was due primarily to the increase in MRA. Angiotensin infused to raise arterial pressure resulted in greater increments in left ventricular than left atrial pressure, so that SPG rose significantly. The increase in RV was due to increases in both MRA and SPG. Norepinephrine infusion increased systolic left ventricular pressure and SPG, while left ventricular end-diastolic pressure and left atrial pressure diminished. Despite a significant increase in SPG, RV did not increase, due to a substantial decrease in MRA. Thus, angiotensin and volume infusion induced a substantial increase in regurgitation due to the increase in MRA, while augmentation of contractility after norepinephrine infusion resulted in a decrease in regurgitation through reduction of MRA. These findings support the clinical view that maintaining a small LV with sustained myocardial contractility will reduce mitral regurgitation. Alternatively, left ventricular dilatation can enhance mitral regurgitation by increasing the effective regurgitant orifice independent of SPG.
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PMID:Dynamic aspects of acute mitral regurgitation: effects of ventricular volume, pressure and contractility on the effective regurgitant orifice area. 44 20

Simultaneous measurements were made of spike activity and perfusion pressure (PA) in intact segments of rabbit middle cerebral artery in vitro. The segments were mounted on a Teflon tube designed so that the perfusing solution flowed in the annular space between the tube and the artery wall, thus magnifying the PA changes occurring when the artery constricted or dilated. A widened portion of the Teflon tube immobilized 1--2 mm of the artery segment for electrical recording with fine glass microelectrodes. Spontaneous spike activity (extra- and intracellular) was regularly observed. When a steady PA and spike discharge was obtained, tests were performed by substituting for the normal perfusion liquid, solutions containing 5 microgram/ml norepinephrine, 5 microgram/ml angiotensin II or 7.5 microgram/ml isoproterenol. Norepinephrine and angiotensin each increased spike frequency (+ 293 and + 126%) and PA (+ 6.6 and + 7.9 mm Hg) whereas isoproterenol decreased spike frequency (-89%) and PA (-22.9 mm Hg). These results a) confirm the presence of receptors to these agents in pial arteries, and b) demonstrate a high degree of correlation between membrane electrical events and mechanical activity of these spontaneously-active myovascular cells.
Stroke
PMID:Correlated electrical and mechanical responses of isolated rabbit pial arteries to some vasoactive drugs. 52 15

Experiments were performed on 19 anaesthetized open-chest dog instrumented with polyethylene catheters inserted: into the aorta, in pulmonary artery and in left atrium and with an electromagnetic flow-transducer placed around the ascending aorta in order to record : systemic arterial and pulmonary pressures, mean left auricular pressure and phasic aortic flow. Heart rate, stroke volume, total systemic and pulmonary resistance, cardiac work were moreover calculated. Each dog was given intravenously by slow infusione : Dopamine (micrograms 5--10--20/kg/min/ 5 min), Isoproterenol (microgram 0.125--0.25--0.5/kg/min/5 min) and Norepinephrine (microgram 0.25--0.5--1 /kg/min/5 min). Results obtained on systemic hemodynamics agree with those reported by many other investigators. On pulmonary circulation : Isoproterenol, at the tested doses, elicited vasodilator effects, Norepinephrine increased total pulmonary resistance but not pulmonary vascular resistance, while Dopamine did not modify or slightly reduced vascular pulmonary tone.
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PMID:[Effects of dopamine, noradrenaline and isoproterenol on pulmonary circulation in anesthetized dogs]. 55 Aug 77

The release of prostaglandin E elicited by sympathomimetic amines was studied in the isolated rabbit heart. The hearts were prepared according to Langendorff, with conventional recording of stroke frequency and contractile force. Assays were made of the outflow of PGE during exposition to equimolar concentrations of methoxamine, noradrenaline, adrenaline and isoprenaline, in the absence and in the presence of phentolamine or propranolol. Noradrenaline caused an almost four-fold increase in the basal outflow of PGE from the heart, while methoxamine (an alpha-adrenoceptor agonist) and isoprenaline (a beta-adrenoceptor agonist) were both ineffective in this respect. Thus, the PGE-releasing capacity of the drugs was not correlated to their ability to activate alpha- or or beta-adrenoceptors. Furthermore, no relation was obtained between the PGE release induced by the drugs and the increase in heart rate and contractile force elicited by them. It is suggested that sympathomimetic drugs trigger PGE synthesis and release in the rabbit myocardium following activation of a hitherto unobserved adrenoceptive mechanism, optimally stimulated by NA.
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PMID:Prostaglandin-mediated inhibition of noradrenaline release: IV. Prostaglandin synthesis is stimulated by myocardial adrenoceptors differing from the alpha- and beta-type. 64 81

Prostaglandin F2alpha constricted pial arterioles when locally applied to the cerebral surface. Norepinephrine and serotonin each elicted similar contractile effects. The constriction produced by F2alpha in combination with either biogenic amine was greater than the constriction elicited by F2alpha or amine acting alone. The effect of one agent on the other was additive rather than potentiating. Since F2alpha norepinephrine and serotonin are all naturally occurring agents, it is possible that their combined effect is important under pathological circumstances and this combined effect should not be overlooked in the search for single spasmogens of great potency. Before ascribing a pathologically important effect of F2alpha, either alone or in combination, evidence is required showing that doses effective in experiments are similar to the concentrations occurring during disease states and/or that vessels may become hypersensitive to F2alpha during such states.
Stroke
PMID:Constriction of pial arterioles produced by prostaglandin F2alpha. 115 64

1. The effects of epinine or dopamine (both 1-10 micrograms kg-1 min-1) on systemic haemodynamics and plasma concentrations of catecholamines and prolactin were studied in conscious pigs before and after combined non-selective alpha- and beta-adrenoceptor blockade. 2. The plasma concentrations of the two compounds did not differ from each other over the entire dose-range. 3. Epinine increased aortic blood flow (AoBF, 24 +/- 6%), which was due to an increase in heart rate (HR) for doses less than 10 micrograms kg-1 min-1. At 10 micrograms kg-1 min-1, HR decreased slightly (10 +/- 3%, as compared to the value obtained at 5 micrograms kg-1 min-1) and stroke volume increased up to 15% (P < 0.05). Mean arterial pressure (MAP, 99 +/- 3 mmHg at baseline) decreased dose-dependently (14 +/- 2%, P < 0.05) up to the infusion rate of 5 micrograms kg-1 min-1, but increased by 4.0 +/- 1.8 mmHg during infusion of 10 micrograms kg-1 min-1. Systemic vascular resistance (SVR) decreased up to 23 +/- 3% for doses less than 10 micrograms kg-1 min-1, but did not change further during infusion of the highest dose. LVdP/dtmax increased during the two highest infusion rates up to 22 +/- 6% (P < 0.05). After the infusion was stopped there was an abrupt increase in HR (18 +/- 4%, P < 0.05) and a further decrease in SVR before all parameters returned to baseline.4. Dopamine caused increases in AoBF (27 +/- 3%) similar to epinine, the only difference being that HR continued to increase (32 +/- 5%) and MAP (13 +/- 3%) and SVR continued to decrease (31 +/- 3%) over the entire dose-range. The increase in LVdP/dt,,,, at the highest dose (48 +/- 4%, P <0.05) was more pronounced than with epinine.5. Adrenoceptor blockade inhibited all epinine-induced changes, but did not affect the dopamineinduced changes in AoBF, SVR and MAP, but attenuated the increases in HR and LVdP/dtmax.6. Noradrenaline (NA) and adrenaline (Ad) concentrations did not change during infusion of epinine or dopamine, but NA increased by 50% within 2.5 min after stopping the infusion of epinine. After adrenoceptor blockade NA and Ad concentrations did not change during infusion of dopamine, which contrasted with a decrease of 55 +/- 5% (P<0.05) in NA during infusion of epinine.7. Prolactin concentrations decreased gradually from 480 +/- 40 pg ml-' to 270 +/- 50 pg ml1' (P<0.05) during infusion of epinine, but did not change significantly during dopamine infusion.8. The differential effects of epinine and dopamine on MAP, SVR, plasma NA (before and after adrenoceptor blockade) and prolactin, leads us to conclude that in conscious pigs, epinine is a more potent a, P2 and D2-receptor agonist, but a weaker D,-receptor agonist than dopamine.
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PMID:Differential cardiovascular and neuroendocrine effects of epinine and dopamine in conscious pigs before and after adrenoceptor blockade. 133 Jan 72

The infusion of prostaglandin E1, a vasodilating substance with predominant effects on the pulmonary vasculature, has been found effective in the management of pulmonary hypertension associated with various diseases. The reported experience with prostaglandin E1 after cardiac transplantation is, however, limited. We used prostaglandin E1 in 18 patients in whom acute right ventricular failure developed after orthotopic cardiac transplantation. The infusion was started within 24 hours after operation in 16 patients and was continued for up to 7 days. Maximal doses of prostaglandin E1, administered via a central venous catheter, ranged from 30 to 120 ng/kg/min. Norepinephrine was simultaneously infused via a left atrial catheter in 10 patients to prevent a reduction in systemic arterial pressure. The prostaglandin E1 infusion resulted in significant reductions in mean arterial pressure and pulmonary vascular resistance and simultaneous increases in cardiac index and stroke index. Mean arterial pressure was stable and left ventricular stroke work increased. The alveolar oxygen tension/forced inspiratory oxygen index tended to decrease during the infusion. Three patients died, two of right heart failure and one of multiple organ failure associated with cardiac allograft rejection. In patients in whom right ventricular failure associated with pulmonary hypertension develops after cardiac transplantation, prostaglandin E1, combined with norepinephrine whenever the arterial pressure declines, can effectively reduce pulmonary artery pressures and improve global cardiac function without compromising systemic perfusion.
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PMID:Prostaglandin E1 infusion for right ventricular failure after cardiac transplantation. 830 1

Doppler echocardiographic transmitral peak early velocity normalized to the time-velocity integral during diastole is equivalent to volumetric peak filling rate normalized to stroke volume. To compare the pathophysiologic validity of normalized and nonnormalized peak early flow velocity, pulsed Doppler echocardiography with simultaneous high fidelity left ventricular pressure measurements was performed in 52 patients with coronary artery disease. Left ventricular loading conditions were changed by intravenous administration of norepinephrine in 15 patients and synthetic atrial natriuretic polypeptide in 15 others. Norepinephrine increased nonnormalized and normalized peak early flow velocities in association with significantly elevated end-diastolic, peak systolic and mitral valve opening pressures and decelerated the time constant of left ventricular isovolumetric pressure decline. Atrial natriuretic polypeptide did not change either nonnormalized or normalized peak early flow velocity, despite significant reductions in end-diastolic, peak systolic and mitral valve opening pressure and an accelerated time constant. Normalized peak early flow velocity showed the highest univariate correlation with long-term change in mitral valve opening pressure (n = 52, r = 0.67, p less than 0.0001). It provided a modest univariate correlation (n = 30, r = 0.74, p less than 0.0001) with immediate change in mitral valve opening pressure during norepinephrine infusion, whereas this correlation was lower (n = 30, r = 0.57, p less than 0.001) during polypeptide infusion. However, multivariate regression analysis relating normalized peak velocity with long- and short-term changes in end-diastolic, peak systolic and mitral valve opening pressures, time constant and constant of left ventricular chamber stiffness improved the correlation coefficients (r = 0.80 to 0.85, all p less than 0.0001). In contrast, neither univariate nor multivariate correlations of nonnormalized velocity with long- and short-term changes in these hemodynamic variables were satisfactory. Thus, nonnormalized peak early flow velocity does not directly reflect underlying hemodynamic changes in humans. Normalization to mitral stroke volume clarifies the dependence of peak early flow velocity on the determinants of early diastolic filling. When left ventricular early diastolic filling is evaluated by Doppler echocardiography, normalized peak early flow velocity should be taken into consideration.
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PMID:Doppler echocardiographic transmitral peak early velocity does not directly reflect hemodynamic changes in humans: importance of normalization to mitral stroke volume. 203 83

To study the haemodynamic and neurohumoral effects of nisoldipine (2 X 10 mg) vs captopril (3 X 25 mg), 24 patients with heart failure (New York Heart Association class II and III) due to coronary artery disease were treated in a randomized double-blind trial over 3 months. Both drugs were well tolerated. Clinical status was similarly improved in both groups, nisoldipine exerted an additional antiischaemic effect. Nisoldipine lowered the mean arterial pressure and capillary wedge pressure acutely and also after long-term treatment. The increase in cardiac index and stroke volume index, however, which was pronounced after acute administration, was no longer present after 3 months of therapy at rest and was abolished during exercise. Norepinephrine plasma concentration increased after the first dose, plasma renin activity did not change, and aldosterone plasma concentration showed a small insignificant decrease. Urine concentrations of norepinephrine and vasopressin were slightly elevated after the 3-month therapy. After captopril, mean arterial pressure and pulmonary capillary wedge pressure decreased acutely and at follow up. Cardiac index and stroke volume index increased significantly only during exercise at follow-up. Plasma renin activity was significantly elevated and aldosterone plasma concentration only slightly lowered. In contrast to what was seen with nisoldipine, plasma norepinephrine concentration and urine catecholamine and vasopressin concentrations remained unchanged. In conclusion, the pronounced haemodynamic effects seen after the first dose of nisoldipine are mostly abolished after long-term treatment, probably due to neurohumoral counterregulation. The haemodynamic response to captopril is complete only after long-term treatment, without evidence of activation of the neurohumoral systems.
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PMID:Acute and long-term haemodynamic and neurohumoral response to nisoldipine vs captopril in patients with heart failure: a randomized double-blind study. 168 8

After completion of abdominal aortic graft, 29 patients received an i.v. infusion of placebo (n = 16) or clonidine 7 micrograms kg-1 (n = 13) over 120 min in a double-blind study. Cardiovascular variables were measured and plasma samples obtained up to 5 h after arrival in the recovery room, for assay of noradrenaline, adrenaline, vasopressin and renin concentrations. Noradrenaline, adrenaline and vasopressin concentrations decreased in the clonidine group throughout recovery (P less than 0.001, 0.05 and 0.05, respectively, vs placebo). Heart rate was less in the clonidine group (P less than 0.01). There was no significant difference in mean arterial pressure between groups. Stroke volume was larger (P less than 0.01) and there were fewer episodes of hypertension (P less than 0.05) and tachycardia in the clonidine group. In addition, a reduction in the number of circulatory interventions (P less than 0.05) and episodes of shivering was noted in the clonidine group. Mean (SD) postoperative volume requirements were larger in the clonidine group (total postoperative input: clonidine 1462 (604) ml; placebo 1064 (348) ml (P less than 0.05]. These data are consistent with the observation that clonidine modifies endocrine and circulatory status after major surgery.
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PMID:Effect of clonidine on the circulation and vasoactive hormones after aortic surgery. 199 45


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